Binding of CXCL8/IL-8 to Mycobacterium tuberculosis Modulates the Innate Immune Response

Interleukin-8 (IL-8) has been implicated in the pathogenesis of several human respiratory diseases, including tuberculosis (TB). Importantly and in direct relevance to the objectives of this report quite a few findings suggest that the presence of IL-8 may be beneficial for the host. IL-8 may aid wi...

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Main Authors: Agnieszka Krupa, Marek Fol, Bozena R. Dziadek, Ewa Kepka, Dominika Wojciechowska, Anna Brzostek, Agnieszka Torzewska, Jaroslaw Dziadek, Robert P. Baughman, David Griffith, Anna K. Kurdowska
Format: Article
Language:English
Published: Wiley 2015-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2015/124762
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author Agnieszka Krupa
Marek Fol
Bozena R. Dziadek
Ewa Kepka
Dominika Wojciechowska
Anna Brzostek
Agnieszka Torzewska
Jaroslaw Dziadek
Robert P. Baughman
David Griffith
Anna K. Kurdowska
author_facet Agnieszka Krupa
Marek Fol
Bozena R. Dziadek
Ewa Kepka
Dominika Wojciechowska
Anna Brzostek
Agnieszka Torzewska
Jaroslaw Dziadek
Robert P. Baughman
David Griffith
Anna K. Kurdowska
author_sort Agnieszka Krupa
collection DOAJ
description Interleukin-8 (IL-8) has been implicated in the pathogenesis of several human respiratory diseases, including tuberculosis (TB). Importantly and in direct relevance to the objectives of this report quite a few findings suggest that the presence of IL-8 may be beneficial for the host. IL-8 may aid with mounting an adequate response during infection with Mycobacterium tuberculosis (M. tb); however, the underlying mechanism remains largely unknown. The major goal of our study was to investigate the contribution of IL-8 to the inflammatory processes that are typically elicited in patients with TB. We have shown for the first time that IL-8 can directly bind to tubercle bacilli. We have also demonstrated that association of IL-8 with M. tb molecules leads to the augmentation of the ability of leukocytes (neutrophils and macrophages) to phagocyte and kill these bacilli. In addition, we have shown that significant amount of IL-8 present in the blood of TB patients associates with erythrocytes. Finally, we have noted that IL-8 is the major chemokine responsible for recruiting T lymphocytes (CD3+, CD4+, and CD8+ T cells). In summary, our data suggest that the association of IL-8 with M. tb molecules may modify and possibly enhance the innate immune response in patients with TB.
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spelling doaj-art-d134461b62d447c6afd185eba5c851e42025-02-03T05:59:56ZengWileyMediators of Inflammation0962-93511466-18612015-01-01201510.1155/2015/124762124762Binding of CXCL8/IL-8 to Mycobacterium tuberculosis Modulates the Innate Immune ResponseAgnieszka Krupa0Marek Fol1Bozena R. Dziadek2Ewa Kepka3Dominika Wojciechowska4Anna Brzostek5Agnieszka Torzewska6Jaroslaw Dziadek7Robert P. Baughman8David Griffith9Anna K. Kurdowska10Department of Cellular and Molecular Biology, University of Texas Health Science Center at Tyler, Tyler, TX 75708, USADepartment of Immunology and Infectious Biology, University of Lodz, 90-237 Lodz, PolandDepartment of Immunoparasitology, University of Lodz, 90-237 Lodz, PolandDepartment of Immunology and Infectious Biology, University of Lodz, 90-237 Lodz, PolandDepartment of Immunology and Infectious Biology, University of Lodz, 90-237 Lodz, PolandInstitute of Medical Biology, Polish Academy of Sciences, 93-232 Lodz, PolandDepartment of Immunobiology of Bacteria, University of Lodz, 90-237 Lodz, PolandInstitute of Medical Biology, Polish Academy of Sciences, 93-232 Lodz, PolandDepartment of Medicine, University of Cincinnati Medical Center, Cincinnati, OH 45219, USADepartment of Medicine, University of Texas Health Science Center at Tyler, Tyler, TX 75708, USADepartment of Cellular and Molecular Biology, University of Texas Health Science Center at Tyler, Tyler, TX 75708, USAInterleukin-8 (IL-8) has been implicated in the pathogenesis of several human respiratory diseases, including tuberculosis (TB). Importantly and in direct relevance to the objectives of this report quite a few findings suggest that the presence of IL-8 may be beneficial for the host. IL-8 may aid with mounting an adequate response during infection with Mycobacterium tuberculosis (M. tb); however, the underlying mechanism remains largely unknown. The major goal of our study was to investigate the contribution of IL-8 to the inflammatory processes that are typically elicited in patients with TB. We have shown for the first time that IL-8 can directly bind to tubercle bacilli. We have also demonstrated that association of IL-8 with M. tb molecules leads to the augmentation of the ability of leukocytes (neutrophils and macrophages) to phagocyte and kill these bacilli. In addition, we have shown that significant amount of IL-8 present in the blood of TB patients associates with erythrocytes. Finally, we have noted that IL-8 is the major chemokine responsible for recruiting T lymphocytes (CD3+, CD4+, and CD8+ T cells). In summary, our data suggest that the association of IL-8 with M. tb molecules may modify and possibly enhance the innate immune response in patients with TB.http://dx.doi.org/10.1155/2015/124762
spellingShingle Agnieszka Krupa
Marek Fol
Bozena R. Dziadek
Ewa Kepka
Dominika Wojciechowska
Anna Brzostek
Agnieszka Torzewska
Jaroslaw Dziadek
Robert P. Baughman
David Griffith
Anna K. Kurdowska
Binding of CXCL8/IL-8 to Mycobacterium tuberculosis Modulates the Innate Immune Response
Mediators of Inflammation
title Binding of CXCL8/IL-8 to Mycobacterium tuberculosis Modulates the Innate Immune Response
title_full Binding of CXCL8/IL-8 to Mycobacterium tuberculosis Modulates the Innate Immune Response
title_fullStr Binding of CXCL8/IL-8 to Mycobacterium tuberculosis Modulates the Innate Immune Response
title_full_unstemmed Binding of CXCL8/IL-8 to Mycobacterium tuberculosis Modulates the Innate Immune Response
title_short Binding of CXCL8/IL-8 to Mycobacterium tuberculosis Modulates the Innate Immune Response
title_sort binding of cxcl8 il 8 to mycobacterium tuberculosis modulates the innate immune response
url http://dx.doi.org/10.1155/2015/124762
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